Neuroplasticity and Neuro Rehab Flashcards
what are ways the CNS can be damaged (7)
trauma
metabolic disturbances
toxicity
infection
ischemia and infarction
hemorrhage
dz
what is the cellular cascade initiated by CNS lesions
- K+ exits; Na, Cl, Ca enter
- H2O follows Na into cells = edema
- glutamate & aspartate released
- enzyme disturbances follow & free radicals, lipases released
- cell membranes, genetic material in cells are damaged and die w/i 5-10min if O2 & glucose supply not restored
what are glutamate and aspartate and what is their role
cytotoxic
causes additional cell death
how does a TIA fit in w cascade of cellular changes seen after CNS lesions
TIA = stoppage of flow, had deficits and then flow resumed
- stoppage so long that level of cell death was accelerated
how does CNS “shock” present in the acute stages (5)
altered LOC
hypotonia
motor and sensory changes
cognitive deficits
decline in function
what is the pathophys behind CNS “shock” in acute stages
absence or slowing of neuron firing
what is the ischemic zone or core of a CNS lesion
directly damaged
what is the penumbra of a CNS lesion
area adjacent to ischemic core
- outer rim
can be damaged also
dec activity and availability of certain enzymes
what is the diaschisis
reduced activity in other parts of the CNS d/t loss of connectivity and communication w lesioned area(s)
what is the time line of the existence of CNS shock
lasts 5ish days
- get tone afterward
what is the goal of medical management when recovering from a CNS lesion
restore blood flow to ischemic core and penumbra as quickly as possible
how is blood flow restored to tissue in the penumbra and what is the significance of this
collateral circulation
collateral flow can only meet energy demands for several hours
what are 2 important considerations when medically managing a CNS lesion
edema has to be managed
ICP regulated
how can the ICP be regulated
meds (TPA)
craniectomy
what specifically allows for the recovery of CNS lesions
neuroplasticity
why can recovery occur spontaneously
edema subsides
metabolic pathways restored
what does the evidence show for PT when recovering from CNS lesions
PT can inc rate and degree of recovery and neuroplastic changes
- want to be aggressive in acute/intense phase
neuroplasticity
ability of nervous system to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function, and neuronal connections
what are two processes that allow for neuroplasticity in the presence of CNS lesions
- neural connections vary in response to environment/stimuli, activity, demands, cellular environment
- cellular mechanism for brain to encode learning and recover from lesions
what should be avoided while healing
sugars/salts - dec metabolic healing
stressful environments
when is neuroplasticity greatest
greatest rate in fetal stage to 2yo
- capability declines w aging but still possible
would there be lasting deficits from a childhood trauma
prob not functionally
may present cognitively
what are methods of imaging for assessing neuroplasticity
fMRI
SPECT
PET
what is neurogenesis
formation of new neurons throughout lifespan
how does neurogenesis change w age
fairly limited in adult mammals
where is neurogenesis more prominent
dentate gyrus of hippocampus
what happens in the hippocampus
learning and memory process
what is synaptic uncovering
chemically induced activity in previously inactive synapses
recruitment of formerly “silent” synapses
what is synaptogenesis
formation of new synaptic connections via axonal sprouting
reactive vs regenerative synaptogenesis
reactive - from nearby, healthy axons
regenerative - damaged axon
what is the goal of cortical remapping
functional substitution
what is cortical remapping
intact regions of the cortex assume the function of damaged areas
how can cortical remapping be assessed on imaging
fMRI
- what part of the brain lights up to complete a task (how was it restructured)
what are 4 mechanisms of neuroplasticity
neurogenesis
synaptic uncovering
synaptogenesis
cortical remapping
what is BDNF
brain derived neurotrophic factor
highly abundant neurotrophin in mammal brains
what is BDNF a key protein for
neuroplasticity processes
- helps to aid in neuroplasticity
what can impact BDNF levels and activity
physical activity inc levels
genetic polymorphisms affect BDNF activity and neuroplastic potential
spontaneous recovery mechanisms are limited to what? what is the impact of this?
10 wks after stroke
- inflammation reduced and metabolic pathways restored
this is where the 3hrs a day model is from
- high levels of intense and meaningful rehab
how can plasticity be harmful
reliance on unaffected side associated w neuroplastic changes may limit engagement of impaired side and results in learned non-use
what is neurorehabilitation
goal based motor training for recovery of impaired or lost motor function
since healing happens whether we do anything or not, what do we want to do w our interventions
want restructuring to be helpful, not harmful
- ms properly aligned, good blood flow to cells in the area
what is the goal of neurorehab when it comes to fostering recovery
foster recovery via neuroplasticity whenever possible
what cases do you see better potential for neuro rehab in
focal, stable lesions
early stages of some progressive conditions
recovery via neuroplasticity requires active participation in: (3)
- goal directed, challenging activities
- age appropriate and salient activities to inc motivation
- repetition is key
what is difficult ab neuro rehab
no protocols exist and limited agreement
- makes prescription and dosing a challenge
ex: even the typical 3hrs might not be sufficient
acute vs chronic phase of CNS lesion
acute - steep recovery curve in 3-6mo period
chronic - after 6mo
how does the rate of recovery change in acute vs chronic stages
rate of recovery slows in chronic phase
- still possible
if there has been a period of semi-automatic recovery, what does this mean for neuroplasticity
can still be induced after this period
what are 6 additional considerations for neuroplasticity
age
nature of lesion
co-morbidities
PLOF
cognition, motivation, mood
genetic factors
what does age mean for neuroplasticity
younger is better
how can the nature of the lesion impact neuroplasticity
focal vs global
- focal is one point (better)
- global - everywhere, harder to nail down
stable vs progressive
- stable - TBI/stroke (better)
- progressive - evolving, ie MS
what are comorbidities to consider for neuroplasticity? why are these relevant?
BMI
cardiac/respiratory hx
harder to push them for acute intense therapy
what about PLOF should be considered for neuroplasticity
fitness
activity level
degree of interconnections established
how can CNS lesion impact motivation
poor motivation
- where injury is can cause depression
- having brain injury itself can be hard to cope w
good motivation in unsafe context
- people might not realize have a brain injury
why genetic factors should be considered for neuroplasticity
how are they going to heal
how well will they heal
what are components/strategies of neurorehab that promote neuroplastic changes
applied motor learning principles
- practice schedules
- feedback
- environment
prevent learned non-use
- CIMT
use of tech
- VR, robotics
- motor imagery
what role does environment paly in creating neuroplastic changes
more challenging vs easier environments
- d/t noise, dynamic, business
what is CIMT
constraint induced movement therapy
forced used of involved limb
- uninvolved limb is constrained via sling, oven mit, etc. and involved limb engaged in challenging and meaningful tasks
evidence for CIMT and recovery
strong
who is CIMT appropriate for
people w weakness in involved and not complete paralysis
what can BWSTT be combined w in training
VR or robotics
what is BWSTT
body weight support treadmill training
allows PT to facilitate normal gait pattern safely, more steps per session, improved body mechanics but may require more staff
research and BWSTT?
effective but no more so than overground training
what can robotic neurorehab devices be used for specifically
training tool and mechanism
evidence for robotic neurorehab devides
good evidence but costly and not widely available
- requires specialized training of PT
what systems does VR tap into
emotional and motivational systems
what is VR and how is it applied in therapy
virtual reality
immersive, 3D, computer-generated environment
interact w or manipulate objects in virtual setting, thereby creating a safe and controlled milieu for therapy sessions
what population has VR been especially effective in?
peds
how is VR effective for neurorehab
inc motivation and compliance which promotes neuroplasticity and recovery thru inc reps of activities
why has there been an inc use of VR in neurorehab
recent dec in cost for systemes
emergence of commercially available serious games
what is rTMS
repetitive transcranial magnetic stim
rTMS to motor cortex can inc excitability of affected hemisphere and inhibit unaffected hemisphere to promote balance and functional reorganization
how does neuroplasticity change over stages of injury as evidenced by TMS mapping of corticospinal system
different neuroplastic mechanisms may occur at different stages
how does rTMS work
magnet placed over area of damage or the opposite side (depending on communication)
- depression on active side
- active side no longer inhibiting actions on other side of brain
- other side of brain can continue inhibiting the active side and further depresses it
where can FES be used
long term to compensate for motor loss, inc safety and independence
- ie lack of DF in gait
literature and FES
varied findings for recovery
what is required for motor imagery to work
intact cognition
what is a pro of motor imagery
free
no special training
what does motor imagery activate
same motor pathways as physical movement
similar physiological responses to overt movement
why do you always want to do motor imagery
every time you think ab doing the action, the neuronal pathway is trying to push thru to the ms and do it
- eventually “plow thru snow pile” and will activate ms (hopefully)
what is regen med and rehab
interprofessional field of research and clinical practice for repair, replacement or regen of cells, tissues, and/or organs in order to restore function lost due to dz or damage
what has led to a rapid proliferation of research in regen med and rehab
recent advances in stem cell and tissue engineering tech
what are limitations to regen med
survival and appropriate differentiation of implanted cells as well as limiting proliferation
who is a good candidate for regen med and stem cell implantation
stable (not too much inflammation or bleeding)
correct genetic programming to convert available STEM cell into cell it needs to be
- don’t want to let it proliferate too much
what is regen med looking for in pts
if there is additional STEM cells or nerves to regen
regen med: studies show greater recovery in who
greater recovery w combination of stem cell plus rehab
rather than either approach used in isolation in animal model studies
pt w too much inflammation and bleeding means what for rehab
focus on stabilizing them medically than PT rehab
what instances in pts are you thinking that recovery isn’t possible
global deficits
dec level of arousal and awareness
advanced, progressive dz or neurodegenerative process
if recovery isn’t possible, what does this mean for rehab
look for ways to compensate or substitute
compensation vs substitution
compensation - use of AD, w/c, AFO to mobilize
substitution - can’t do motion you want, but use other ms to create different movement to reach the same goal
what are examples of substitutions
tenodesis grasp (often in SCI)
- use automatic finger flex when extend wrist to pick something up
circumduction in swing phase of gait d/t loss of rectus fem
